Case study/ advanced pathophysiology

Casestudy/ advanced pathophysiology

Casestudy C

Pathogenesisof ascites in the patient, who displays the onset of portalhypertension.

Ascitesis a pathologic amassing of fluid in the peritoneal cavity. Thecondition is the most common complication of cirrhosis. Thepathogenesis of ascites is the consequence of a series ofpathophysiological, anatomical as well as biochemical abnormalitiesthat occur in patients (Gorelicket al.2011).The patient in the case study exhibited portal hypertension, acondition linked to the development of ascites. In the case study,the patient exhibits a shrunken heterogeneous liver. At the sametime, the patient confesses to being an alcoholic. Alcohol is a majorcause of liver failure. The development of portal hypertension is thepreliminary step that contributes to fluid retention in the settingof cirrhosis. The development of cirrhosis is divided into apreclinical phase and clinical phase. The first phase is usuallyprolonged. Portal hypertension is important in the transition fromthe preclinical to the clinical phase of cirrhosis. Portalhypertension contributes to an increase in both the intrahepaticvascular resistance and portal venous inflow (Iwakiri,2014).The intrahepatic vascular resistance is as a result of architecturaldistortion of the liver that results from fibrosis, and an increasedsinusoidal tone. Portal inflow in the veins results from acombination of an increased plasma volume and a hyperdynamiccirculatory state. In the patient’s case, the collateralcirculation developed by the opening of preexisting vascular channelsand by neo-formation of vessels, in response to the increased portalpressure. The esophagogastric varices are important collateralvessels that increase their sizes with an increase in portal pressureand breaks when the critical tension value is exceeded. The rapturemay cause bleeding that may further result in the death of thepatient.

However,it is important to note that ascites do not develop only in thosepatients with portal hypertension. They can also develop in patientswith hepatocyte failure but no hypertension. A good example is thosethat develop as results of liver failure caused by cancers. This typeof condition is known as malignant ascites. These ascites arestipulated to be linked to a combination of interfered vascularperviousness together with obstructed lymphatic drainage. Fivedifferent barriers exist that prevent the movement of proteins awayfrom the intravascular space. These barriers are interstitialstroma, mesothelium basement membrane, capillary endothelium,mesothelial cells lining the peritoneal, and the membrane of thecapillary basement. These five parts work in conjunction with thetight junction and the anionic macromolecules to maintain thebarrier. These prevent the leakage of protein molecules into thecavity of the peritoneal.

Sincecells, macromolecules and proteins do not normally leave theintravascular space they return to the systemic circulation by theperitoneal lymphatic system. The pathway starts with the lymphaticstomata, then enters the peritoneal lymphatic through the diaphragm,and then undergoes filtration through the regional lymph nodes.Finally, the system ends with the emptying into the thoracic duct.All these happens through the osmotic gradient. It is the obstructionof the peritoneal cavity that is associated with the development ofmalignant ascites. A tumor can destroy the peritoneal cavity makingthe fluid unable to return to into the intravascular space.

Inconclusion, it is evident that there is a total difference in howascites develop from patients with portal hypertension and those withNO portal hypertension. Of great importance is that the quality offluid in those patients with malignancy-related ascites isdistinctive and has a high ascetic concentration of fluid protein andlow gradient of serum-albumin.

CaseStudy D

Parkinson’sdisease is a neurological disorder involving only a few predisposednerve cell types in certain regions of the nervous system. Theintra-cerebral development of abnormal proteinaceous Lewy bodiestogether with Lewy nutrites starts at specific induction sites andmoves in a topographically predictable sequence. As the Parkinson’sdisease progresses, components of the autonomic, somatomotor systemsand limbic systems become badly destroyed. In the presymptomaticphases one and two, inclusion body pathology is contained in themedulla oblongata and the olfactory bulb. In the last phases, thesubtantia nigra together with the other nuclear grays of the midbrainare the focus of the initial slight and, then, severe changes. Atthis phase, most patients cross the threshold to the symptomaticphase of the disease. In the final stages five and six, thedevelopment process of the disease enters the mature neocortex, wherethe disease manifests itself into all of its known clinical forms.

Parkinsonism(pseudo Parkinson`s disease), on the other hand, is a neurologicaldisease that results in the slowness of movements(Hieber, 2012).It is a clinical syndrome resembling Parkinson’s disease usuallyinduced by the dopamine receptor antagonist property of neurolepticantipsychotic drugs. The term pseudo may be used to imply that themotor dysfunction resembles but is not what appears in Parkinson’sdisease. The motor dysfunction does not relate to nigrostriataldysfunction.

Inboth cases of Parkinson’s disease and pseudo-Parkinson’s disease,the patients appear rigid, slow and exhibit a shuffling gait. Thesimilarity in clinical appearance is as a result of apraxic slowness,frontal gait, and slowness disorder (Kurlan,&amp Rabin, 2013).Apraxia is the inability of the patient to perform due to slowedcognitive processing. The condition results from a disturbance ofcortical association function leading to the appearance of akinesia,hypokinesia, and bradykinesia. Akinesia is the failure of willedmovements to occur hypokinesia is the reduced amplitude of movementwhile bradykinesia is the slowness of movements(Kurlan, &amp Rabin, 2013).The bradykinesia effect in Parkinson’s disease that can be seenthrough repetitive finger movements cannot be seen inpseudo-Parkinson’s disease.

Neuro-cognitivestudies can help in distinguishing the two conditions. There isrigidity in pseudo-Parkinson disease, and it depends on the speed ofmovement (Sorondet al. 2011).In other words, the rigidity is greater in faster movement and lessin slow movements. In contrast, in Parkinson’s disease, the degreeof rigidity is not dependent on the speed of movement. Anotherdifference that distinguishes these two conditions is that inParkinson’s disease there is additional festination andretropulsion.

Belowis a table that summarizes the distinguishing features of Parkinson’sdisease and pseudo-Parkinson’s disease, including both the motorand non-motor symptoms.

Parkinson’s disease

Pseudo-Parkinson’s disease

Is characterized by bradykinesia

Patients have a resting tremor

Patients have lead pipe rigidity

The patients are characterized by postural instability

The patients have shuffling gait with festination, and exhibits retropulsion.

Is characterized by apraxic slowness

Patients have essential tremor, myoclonus

Patients have paratonic rigidity

The patients have frontal ataxia

The patients exhibit a shuffling apraxic gait.

Insummary, there are several cases of misdiagnosis of the twoconditions, pseudo-Parkinson, and Parkinson’s disease, because oftheir close resemblance. Therefore, it is important for the nursingpractitioners to know the existing difference between actualParkinson’s disease and pseudo-Parkinson’s disease so as toreduce these cases of misdiagnosis.


Dodge,H.H., Mattek, N.C., Austin, D., et al. (2012) In home walking speedand variability trajectories associated with mild cognitiveimpairment. Neurology, 78, 1946- 1952.

Gorelick,P.B., Scuteri, A., Black, S.E., et al. (2011) AHA/ ASA ScientificStatement: Vascular contributions to cognitive impairment anddementia. Stroke, 42, 2672-2713.

Hernández-Gea,V., Aracil, C., Colomo, A., Garupera, I., Poca, M., Torras, X., … &ampVillanueva, C. (2012). Development of ascites in compensatedcirrhosis with severe portal hypertension treated with β-blockers.TheAmerican journal of gastroenterology,107(3),418-427.

Hieber,R. (2012). Movement disorder toolbox. MentalHealth Clinician,1(7),153-155.

Iwakiri,Y. (2014). Pathophysiology of portal hypertension. Clinicsin liver disease,18(2),281-291.

Kurlan,R., &amp Rabin, M. L. (2013). Pseudoparkinsonism: A review of acommon nonparkinsonian hypokinetic movement disorder. Advancesin Parkinson`s Disease,2013.

McGinn,A.P., Kaplan, R.C., Verghese, J., et al. (2008) Walking speed andrisk of incident ischemic stroke among postmenopausal women. Stroke,39, 1233-1239.

Sorond,F.A., Kiely, D.K., Galica, A., et al. (2011) Neuro-vascular couplingis impaired in slow walkers: The MO-BILIZE Boston study. Annals ofNeurology, 70, 213-220.